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This is reminiscent of our recent study on SCA31, in which we demonstrated a novel role of the ALS/FTD-linked RBPs TDP-43, FUS, and hnRNPA2B1 as RNA chaperones binding to UGGAA repeat RNA and altering its structure, resulting in the suppression of its neurotoxicity through reducing RNA foci formation and repeat polypeptide translation (Ishiguro et al., 2017)

And another is a dominant negative effect the bad copy itself is causing problems its not just nonfunctional, it has some gain of function that lets it do things it wouldnt normally do (like bind different proteins, distracting them from their own jobs), or it hogs up the things the good copy needs without actually being able to use them

n=8, SEM=0.0418